Our results demonstrated (a) elevated NID2 levels in murine steatotic livers and human atherosclerotic vascular tissues, (b) increased hepatic steatosis and fibrosis in NID2-overexpressing mice, (c) exacerbated atherosclerosis in mice with NID2 overexpression, and (d) reduced AMPK activation in the livers of NID2-overexpressing mice. The gene discussed is NID2; the disease is atherosclerosis.